The proposed work attempts to determine which of several mechanisms mediates recovery of behavioral function or sparing from behavioral loss after brain damage. Collateral sprouting, neurochemical adjustments, vicarious function and age are the mechanisms to be studied after lesions are made within a model system whose morphological connections, neurochemistry, pharmacology and behavior have been well characterized. The nigral and frontal cortical (FC) projections to the neostriatum, and the role this triad plays in regulating the rat's ingestive behavior and body weight comprise the model system. Further analysis of the sparing from unilateral lateral hypothalamic (LH) damage that occurred when the ipsilateral FC was ablated 30 days prior to LH lesion will be attempted. Also, preliminary neurochemical, pharmacological and behavioral analysis of the mechanisms which mediate recovery from unilateral LH damage will be extended. After various combinations of lesions of FC, LH and dorsal thalamus, experimental subjects will be observed with behavioral, and light and fluorescence microscopic techniques to determine if sprouting accounts for sparing of ingestive behavior by prior lesions, and to define the neural systems within which the growth occurs. Additionally, after lesions of either FC or LH, observations of spontaneous ingestive behavior or ingestive behavior after varying drug treatments, together with neurochemical assay studies and receptor site binding studies will evaluate the role in recovery and sparing, of spontaneous neurochemical adjustments such as development of denervation supersensitivity and cessation of dopamine leakage from degenerating terminals. Also, the role in sparing and recovery that alternative systems play through vicarious function will be studied after pharmacological blockade of these possible alternative systems. Finally, to determine the dependency of sparing and recovery upon operation of the above mechanisms within nigral and FC projections, the age of the animal will be varied, since these eating systems either are more susceptible to damage or are not functional in young rats.